Bone scintigraphy is of little diagnostic value in the imaging workup of trauma-induced MO, especially when presenting as an isolated soft-tissue mass. However, a bone scan may be ordered when other inflammatory conditions, such as cellulitis, osteomyelitis, or thrombophlebitis, are considered.24 A bone scan will demonstrate increased uptake in injured muscle because of the presence of calcium salts and is the most sensitive imaging modality for detecting heterotopic bone formation in the very early stages.22,24 Several authors have found that three-phase bone scintigraphy is more useful in differentiating MO from other inflammatory conditions compared with a standard bone scan, which generally includes only delayed images.22,24 Although serial bone scans have been suggested to aid in the timing of surgical intervention, the practical application of relying on bone scintigraphy to determine successful treatment is largely unfounded in this setting.22,24 Because increased uptake on a bone scan can be seen chronically in trauma-induced MO, the authors have not found bone scans to be a reliable test for determining either the timing of surgical excision or for predicting the theoretic risk of recurrence (Figure 5).
CT is the best modality for delineating the zonal pattern of calcification and can be diagnostic before the characteristic calcification pattern becomes radiographically detectable.25,26 In the initial stages, CT demonstrates soft-tissue swelling or a low-attenuation soft-tissue mass without associated calcifications. Typically the peripheral rim becomes increasingly calcified as it matures (Figure 3). The central lucent zone is typically isodense to adjacent muscle.25 However, if the peripheral zonal pattern is not evident, it may be difficult to diagnose MO reliably by CT alone, necessitating additional imaging evaluation or follow-up.
MRI is the best single modality for imaging soft-tissue masses. An MRI for the evaluation of a soft-tissue mass should be interpreted in conjunction with recent radiographs because calcifications may not be well demonstrated on MRI.27 Recently, Papp et al28 discussed the utility of MRI for diagnosing soft-tissue masses. They classified lesions as determinate or indeterminate based on imaging characteristics and clinical presentation. A determinate lesion can be definitively diagnosed by means of history and physical examination combined with appropriate imaging modalities such as MRI. A lesion in a characteristic location (eg, anterior femoral cortex) supports the diagnosis of MO and is, therefore, also an important consideration. By comparison, indeterminate lesions (eg, type of sarcoma) require biopsy for an accurate diagnosis. Because each physician’s experience guides him or her in classifying lesions as determinate or indeterminate, a thorough history and physical examination cannot be understated, and a multidisciplinary team approach is useful for optimizing diagnostic accuracy and minimizing risks associated with further evaluation, including biopsy.29
Although MO can often be diagnosed definitively by MRI, its appearance can vary depending on the histologic stage;30 therefore, other diagnostic considerations must be excluded (eg, soft-tissue sarcoma, abscess). In the acute phase, when hematoma is often present, MO typically demonstrates a heterogeneous signal intensity on T1-weighted areas of high signal intensity that are representative of blood products. Fluid-weighted sequences may also be heterogeneous in appearance. T2-weighted hyperintensity suggests regions of granulation tissue, blood products, and edema. T2-weighted hypointensity may correspond to hemosiderin deposition or calcifications. Lack of lesion enhancement is characteristic when hematoma is present. Although intralesional enhancement has been reported in MO, heterogeneous or solid enhancement should raise the suspicion of sarcoma.31 Furthermore, a rim of bright T1-weighted signal is often suggestive of peripheral methemoglobin; surrounding inflammatory edema may also be present (Figure 6). Gradient-echo sequences can be used to investigate areas of hemosiderin deposition during this stage.31
The MRI appearance that follows the acute phase classically demonstrates a lesion that is isointense to slightly hypointense to skeletal muscle on T1-weighted sequences. Fluid-weighted sequences will appear hyperintense to surrounding muscle. At this stage, surrounding edema may or may not be present. If the zonal pattern of growth, characterized by peripheral low signal intensity, can be identified, this supports the diagnosis of MO and corresponds to a determinant lesion. However, in some instances, the lesion may be subtle and identified only by an alteration in fascial planes, thus stressing the importance of careful examination of the area in question (Figure 3).
As lesions progress, a pattern of mature, lamellar bone becomes better defined and demonstrates low signal intensity on all sequences, and the surrounding edema has resolved. Mature lesions may have areas of internal fat, which correspond to marrow production in the heterotopic bone. If MO is suspected on the basis of MRI, then CT and/or radiographs are recommended to confirm the characteristic peripheral mature calcification.31,32
When MO presents with a characteristic history and a clear zonal pattern on imaging, diagnosis is relatively straightforward. However, it is not uncommon for the appearance of MO to be suggestive of other considerations, thereby making the diagnosis challenging3,7,9,10,18,33 (Table 2). Nuovo et al17 reviewed 23 patients with MO that had “atypical” presentation. Of these 23 patients, 3 presented before the age of 10 years. Fifteen lesions were in unusual locations, including fingers and the chest wall. Only eight of their patients had a history of trauma. Two patients had constitutional symptoms that led to a presumptive diagnosis of infection. In eight of their patients, histology suggested a malignant diagnosis.17 Thus, a malignancy may be suspected despite advanced cross-sectional imaging and biopsy.
In the acute phase of MO, the MRI appearance can simulate a soft-tissue abscess. However, a soft-tissue abscess classically demonstrates a uniform appearance with high signal intensity on T2-weighted sequences, low signal intensity on T1-weighted sequences, and peripheral enhancement on post-contrast images.34 CT with intravenous contrast demonstrates a bright, rim-enhancing fluid collection, often confirming the suspicion of abscess.34
It is also important to distinguish MO from soft-tissue sarcoma, which can have very similar imaging and pathologic characteristics (Figure 4, A). A high level of suspicion is often salient to accurate diagnosis. Atypical presentation (eg, apparent hematoma lacking ecchymosis), intralesional post-contrast enhancement, and calcifications that lack the characteristic zonal pattern of peripheral ossifications may lead the clinician to favor sarcoma.31,32 For example, up to 58% of patients with synovial sarcoma have calcifications evident on diagnostic imaging and generally lack the peripheral rim of ossification that is seen with MO.35 A more mature calcification pattern might also be confused with parosteal osteosarcoma on radiographs alone (Figure 4), highlighting the importance of advanced cross-sectional imaging.35
Less commonly encountered considerations that may have soft-tissue calcifications include reactive periostitis and, when associated with the surface of the bone, bizarre parosteal osteochondromatous proliferation (ie, Nora lesion). Occasionally, a chronic abscess will develop calcification and thickening of its outer wall, which may appear similar to MO.34
Melorheostosis is a rare benign sclerotic bone dysplasia that follows a sclerotomal distribution and is known to have a “myositis-like” variant. The key to differentiate melorheostosis from MO is identification of the sclerotomal pattern, which is not characteristic of MO. One rare but notable mimicker of MO is a soft-tissue recurrence of giant cell tumor of bone. Recurrent giant cell tumor of bone in the soft tissues will often have peripheral eggshell calcifications, which may appear identical to MO.
MO can be classified as a determinate lesion when it presents with a clear history of an inciting event and peripheral calcification on radiographs. However, in early lesions, radiographs may be nondiagnostic, and subsequent MRI findings are often nonspecific. For patients with an indeterminate lesion, a tissue sample is necessary before forming a treatment plan. A biopsy can be performed using a variety of techniques depending on the surgeon’s preference. A fine-needle aspiration, core biopsy, incisional biopsy, and excisional biopsy are all methods that have been used to sample tissue. Regardless of the technique used, it is important for the treating surgeon to be familiar with the limitations of each method and the principles involved with biopsy should malignancy be identified. Fine-needle aspiration for cytology has been reported to be nondiagnostic and was unable to rule out sarcoma in some patients with MO; it is generally not recommended when core tissue samples can be obtained for pathologic analysis.29 Therefore, image-guided core biopsy is the authors’ preferred technique. Moreover, CT guidance is ideal for sampling representative tissue from both the central and peripheral aspects of the lesion.
Incisional biopsy allows direct visualization of the lesion and offers the greatest amount of tissue for analysis, but it is also the more invasive compared to closed needle biopsies. Incisional biopsies may be used when image-guided biopsy is unavailable, after a core-needle biopsy when the diagnosis is uncertain, or when additional tissue is needed. Excisional biopsies are reserved for small, easily accessible lesions when imaging is consistent with a benign etiology. The authors’ recommend a multidisciplinary team approach when considering histological analysis.
The histologic course of MO progresses from an immature, highly cellular fibroblastic lesion to a mature mass with peripheral lamellar bone.7 The timing of this process varies but generally occurs over several weeks and correlates with the development of calcifications on imaging.7,30 Early lesions demonstrate mesenchymal metaplasia, intermediate lesions display mixed chondro-osseous differentiation, and mature lesions demonstrate mature bone.9 In the early stages, it may be difficult microscopically to distinguish MO from sarcoma (eg, extraskeletal osteosarcoma).7,10 Grossly, a mature lesion will present as a thin shell of bone covering a soft red-gray central area7 and is typically 3 to 6 cm in size. Microscopically, MO is characterized by a distinct zonal pattern that correlates to its stage of maturity.7,9 Centrally, proliferating fibroblastic tissue and interstitial microhemorrhages are seen. Mild cellular pleomorphism and mitotic activity may be present.7 An intermediate zone has areas of immature woven bone mixed with fibroblastic tissue. At the periphery of the lesion, mature lamellar bone is seen (Figure 7). Although the development of sarcoma in the setting of previous MO has been reported, the ability of MO to transform into sarcoma has been questioned and has not been universally accepted.7
The goal of nonsurgical treatment is to minimize symptoms and maximize function. Nonsurgical treatment is often successful because MO is self-limiting and often is a self-resolving process.14,36 Although well-designed studies are lacking, the observation that MO is more common in patients with bleeding disorders37 supports the hypothesis that MO is associated with hematoma formation, with or without concomitant periosteal injury. Therefore, initial treatment of muscle injury with the purpose of controlling the development of hematoma and maintaining function is a reasonable approach.
For the initial treatment of muscle injury, Järvinen et al37 recommend a brief period of relative immobilization for 3 to 7 days combined with rest, ice, compression, and elevation. Crutches may assist with resting the affected area and minimizing hematoma formation.36,37 Cryotherapy—15 to 20 minutes of ice every 30 to 60 minutes—can decrease intramuscular blood flow by 50%. Aggressive physical therapy should be avoided in the very early stages to prevent exacerbation of symptoms.36,38
Assisted range-of-motion exercises, within a pain-free arc of motion, may begin as early as 48 to 72 hours.39 A gradual progressive exercise program begins with isometric training, followed by isotonic training, and finally isokinetic and dynamic exercises. Large fluctuant and symptomatic hematomas may benefit from aspiration.36 In one series, 42 of 42 football players at Vanderbilt University returned to full participation without loss of function after moderate to severe quadriceps contusion. The authors stressed the importance of early and persistent nonsurgical treatment.36 In more mature lesions, active range-of-motion and resistive strengthening exercises are important to maintain and improve joint range of motion and function.10,36,38
The use of drugs in the prophylaxis of MO after injury is limited and has largely been extrapolated from studies examining the development of heterotopic bone formation after pelvic trauma and hip surgery. However, in a case report of traumatic MO developing in an athlete, two doses of pamidronate were associated with improvement in both the clinical and radiographic findings.40
Surgical excision is generally reserved for symptomatic lesions that have failed nonsurgical treatment. The goal of surgery is to improve function and limit pain. Surgical indications include intractable pain resulting from mechanical irritation of nearby tendons, bursa, or joints; lesions that are causing compression of important neurovascular structures; and decreased range of motion that compromises activities of daily living.38 Marginal excision is adequate, but recurrence has been reported.10
Historically, surgical intervention has been delayed 6 to 18 months following injury because it was thought that surgery does not alter the maturation process and, therefore, premature surgery may predispose to recurrence.15 However, conclusive evidence supporting this approach is lacking.7,10,13-15,38,39 In fact, more recent research has challenged the risk of recurrence with early intervention. Ogilvie-Harris and Fornasier33 reported on 26 patients with nontraumatic MO and suggested that early excision has minimal risk of recurrence. Similarly, Garland15 suggested that the decision when to excise should include the etiology of MO rather than be based solely on chronology. He suggested delaying surgery for 6 months following traumatic MO, 1 year after spinal cord injury, and 18 months following head injury.15
It is possible that the risk of recurrence and severity of MO is dependent on the initial degree of local soft-tissue trauma. Those who present without disclosing a history of trauma may have suffered a mild injury that went unnoticed and may do well with early excision if symptomatic, as opposed to patients who developed heterotopic bone secondary to severe soft-tissue injury (eg, elbow dislocation), who may do better with delayed excision, once the lesion has reached maturity. Therefore, the decision to proceed with surgery is optimized in a multidisciplinary setting, accounting for the etiology, radiographic findings, laboratory values, and patient symptoms.
MO is a self-limiting, reactive, bone-forming process of soft tissues that occurs following injury. It may mimic malignancy early in its development, especially when it is not associated with a characteristic presentation and imaging findings. The pathophysiology is incompletely understood; however, it likely involves the inappropriate differentiation of mesenchymal stems cells into chondrocytes and osteoblasts in an inflammatory-rich environment. Diagnosis is often made with a thorough history, physical examination, and orthogonal radiographs. However, a variety of advanced imaging modalities may be useful depending on the stage of evolution. A biopsy is necessary to confirm the diagnosis for indeterminate lesions. Nonsurgical treatment focuses on reducing symptoms and maximizing function. Surgical excision is reserved for lesions that have failed nonsurgical treatment. The optimal timing of surgical excision is undetermined but has traditionally been felt to be best performed once a lesion has reached maturity. A multidisciplinary approach is helpful to accurately diagnose and optimize treatment.
Evidence-based Medicine: Levels of evidence are described in the table of contents. In this article, references 20 and 32 are level II studies. References 1-3, 6, 14, 17, 19, 21, 22, 26, 27, 29, 33, 35, and 40 are level IV studies.
References printed in bold type are those published within the past 5 years.
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© 2015 by American Academy of Orthopaedic Surgeons
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